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anti-Fas (TNF Receptor Superfamily, Member 6) Antibodies (FAS)

On www.antibodies-online.com are 774 Fas (TNF Receptor Superfamily, Member 6) (FAS) Antibodies from 42 different suppliers available. Additionally we are shipping FAS Kits (91) and FAS Proteins (61) and many more products for this protein. A total of 964 FAS products are currently listed.

Fas single-nucleotide polymorphisms rs2234767 and rs1800682 are involved in the pathogenesis of Idiopathic Aplastic Anemia

The mRNA expression of FAS was lower in patients with TP53 mutation than TP53 wild-type. Our findings suggest that TP53 mutation is a potential negative predictor of metastatic melanoma treated with CTLA-4 blockade.

Complete local landscape for a defined molecular function-the alternative splicing of an exon (FAS/CD95 exon 6). The extensive epistasis in the landscape predicts that exonic regulatory sequences may diverge between species even when exon inclusion levels are functionally important and conserved by selection.

Paper analyses results of serum cytokines and lymphocyte apoptosis study in nodular goiter against the background of autoimmune thyroiditis and thyroid adenoma based on the cell preparedness to apoptosis, the number of apoptotic lymphocytes and the content of proapoptotic tumor necrosis factor-alpha, interleukins in serum, considering the polymorphism of BCL-2, CTLA-4 and APO-1 genes.

These results demonstrated that overexpression of ING4 can induce the apoptosis of melanoma cells and CD3+ T cells through signaling pathways such as the Fas/FasL pathway, and that ING4 gene therapy for melanoma treatment is a novel approach.

These results indicated that cMyc and Fas regulated the sensitivity of A549 cells to irradiation by regulating caspase8-mediated Bid activation and the subsequent association with the mitochondrial pathway of apoptosis.

this study characterized in juvenile systemic lupus erythematosus a distinct profile from adult SLE that comprises increased sFas, sTRAIL, and reduced sFasL, notably in patients with active disease and with nephritis.

results from the current study showed that the association of FAS-670A/G SNP with idiopathic azoospermia was not found in a population of men with idiopathic infertility.

The authors observed differential expression of CD95(Fas) in CD27(+) B-cells from cirrhotic patients that was inversely correlated with peripheral CD27(+) B-cell frequency. They conclude that peripheral CD27(+) memory B-cells in cirrhosis exhibit increased sensitivity to Fas-induced apoptosis in an activation-dependent manner to which endotoxin contributes, associated with reduced frequency of circulating memory B-cells.

the analysis of mRNA level showed that disease progression is associated with significantly increased expression of FasR and/or FasL. In conclusion, our observation seems to confirm that spherical model of cancer lines is more reliable for some sophisticated analysis because of their greater resemblance to the CSCs from human CRC samples in comparison to commonly used adherent cells

study indicates FAS-FASL promoter SNPs may promote the production of cross-reactive anti-ganglioside antibodies in GBS

In primary hyperparathyroidism, hyperplasias demonstrated the highest expression of TRAIL and Fas, whereas in adenomas it was increased compared to normal tissue, but lower than in hyperplasias.

Messenger RNA and protein levels of prostaglandin (PG) E synthase (PGES), PGF2alpha receptor (PGFR), tumor necrosis factor-alpha (TNF) and Fas were found to be higher in the corpus luteum of pregnancy than in corpus luteum of the cycle.

Results did not support that K8/K18 filaments influence the expression of Fas on the surface of luteal cells.

activation of the Fas pathway and presence of FSH during in vitro maturation increased the incidence of apoptosis in cumulus cells

demonstrated for the first time that normal ejaculated spermatozoa express Fas antigen; data showed that a large percentage of normal ejaculated spermatozoa of fertile bulls are immunocytochemically positive for Fas

identification of 14-3-3zeta as a novel phosphocofilin binding protein involved in the maintenance of the cellular phosphocofilin pool

our computational and experimental approach identified Fas as a regulator of the Th17-to-Th1 cell balance by controlling the availability of opposing STAT1 and STAT3 to have a direct impact on autoimmunity.

In conclusion, these data demonstrate that murine herpesvirus 68-immortalized SL-1 cells can be recognized and controlled by specific cytotoxic T cells through CD95/CD95L-mediated apoptosis.

Findings indicate that induction of apoptosis through Fas is dependent on receptor palmitoylation in primary immune cells, and Fas may prevent autoimmunity by mechanisms other than inducing apoptosis.

Both Sharpin/Fas and Sharpin/Fasl compound mutant mice developed an auto-inflammatory phenotype similar to that seen in Sharpin null mice, indicating that initiation of apoptosis by FAS signalling is likely not involved in the pathogenesis of this disease.

leucine deprivation induces the expression of miR-212-5p in a GCN2/ATF4-dependent manner. miR-212-5p suppresses lipid accumulation in liver by targeting FAS and SCD1 under both normal diet and high-fat diet conditions.

Our data show that loss of Fas activity strongly affects the early development of atopic dermatitis (AD) by leading to Th2-dominant inflammation characterized by dermal infiltration of CD4+ T cells, neutrophils and increased skin expression of Th2 cytokines.However, Fas/FasL-apoptotic pathway is also involved in restricting tissue remodelling and dermal fibrosis during AD.

Hrd1-null B cells exhibited high Fas expression during activation and rapidly underwent Fas-mediated apoptosis, which could be largely inhibited by FasL neutralization. Fas mutation in Hrd1 KO mice abrogated the increase in B-cell AICD. We identified Hrd1 as the first E3 ubiquitin ligase of the death receptor Fas and Hrd1-mediated Fas destruction as a molecular mechanism in regulating B-cell immunity.

These findings reveal a role for MOAP-1 in Fas signaling in the liver by promoting MTCH2-mediated tBid recruitment to mitochondria.

The in vivo delivery of CRISPR/Cas9 could maintain liver homeostasis and protect hepatocytes from Fas-mediated cell apoptosis in the fulminant hepatic failure model.

This study demonstrated that Ischemic neurons release sFasL, which contributes to M1-microglial polarization.

results indicate that IL-1beta, produced by the inflammasome and Fas-dependent mechanisms, contributes cooperatively to the Th17/Th1 induction during bacterial infection. This study provides a deeper understanding of the molecular mechanisms underlying Th17/Th1 induction during pathogenic microbial infections in vivo.

K8/K18-dependent PKCdelta- and ASMase-mediated modulation of lipid raft size can explain the more prominent FasR-mediated signaling resulting from K8/K18 loss.

The present results suggest that Fas/S1P1 signaling via activation of NF-kappaB in osteoclast precursor cells is a key factor in the pathogenesis of rheumatoid arthritis in the temporomandibular joint.

The present results may provide some insights to understand the role of Fas/FasL in the spinal cord but not motor cortex with neuronal apoptosis and neuroplasticity in monkeys subjected to hemisection spinal cord injury.

FAS Antigen Profile

Antigen Summary

The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform.